Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet
Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet
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DOI：
10.1007/s00125-005-0053-y
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发表时间：
2006-02-01
期刊：
影响因子：
8.2
通讯作者：
Kopecky, J
中科院分区：
文献类型：
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作者：
Flachs, P;Mohamed-Ali, V;Kopecky, J
目的/假设：富含n-3多不饱和脂肪酸（即二十碳五烯酸（EPA）和二十二碳六烯酸（DHA））的饮食可以防止啮齿动物的胰岛素抵抗和肥胖，并增加健康人的胰岛素敏感性。我们测试了EPA和DHA的抗糖尿病作用是否涉及增加内源性胰岛素增敏剂脂联素的产生。研究方法：我们研究了在促进肥胖的高脂肪饮食中，在5周内用EPA/DHA浓缩物（6%EPA，51%DHA）部分替代植物油对成年雄性C57 BL/6 J小鼠的影响，这些小鼠可以自由获得食物或限制其食物摄入量30%。在治疗结束时，测量脂质和葡萄糖代谢的全身标志物以及全长脂联素和瘦素。对背腰和附睾白色脂肪组织（WAT）和分离的脂肪细胞中的脂联素（Adipoq）和瘦素（Lep）基因表达进行定量，并评价来自WAT外植体的脂肪因子产生。结果如下：在自由获取食物的小鼠中，存在EPA/DHA的情况下，血浆三酰甘油、NEFA和胰岛素水平较低，而葡萄糖和瘦素水平没有显着改变。限食可降低血浆甘油三酯、血糖、胰岛素和瘦素，但不降低脂联素。EPA/DHA增加血浆脂联素水平，与食物摄入无关，反映了脂肪细胞中Adipoq表达的刺激和WAT，特别是附睾脂肪中脂联素的释放。Lep的表达和瘦素从WAT中的释放，虽然对热量限制非常敏感，但EPA/DHA没有改变。结论/解释：摄入富含EPA和DHA的饮食会导致脂联素的全身浓度升高，这在很大程度上与食物摄入或肥胖无关，并在一定程度上解释了其抗糖尿病作用。
Aims/hypothesis: Diets rich in n-3 polyunsaturated fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), protect against insulin resistance and obesity in rodents and increase insulin sensitivity in healthy humans. We tested whether the anti-diabetic effects of EPA and DHA involve enhanced production of the endogenous insulin sensitiser, adiponectin. Methods: We studied the effects, in an obesity-promoting high-fat diet, of partial replacement of vegetable oils by EPA/DHA concentrate (6% EPA, 51% DHA) over a 5-week period in adult male C57BL/6J mice that either had free access to food or had their food intake restricted by 30%. At the end of the treatment, systemic markers of lipid and glucose metabolism and full-length adiponectin and leptin were measured. Adiponectin (Adipoq) and leptin (Lep) gene expression in dorsolumbar and epididymal white adipose tissue (WAT) and isolated adipocytes was quantified and adipokine production from WAT explants evaluated. Results: In mice with free access to food, plasma triacylglycerols, NEFA, and insulin levels were lower in the presence of EPA/DHA, while glucose and leptin levels were not significantly altered. Food restriction decreased plasma triacylglycerols, glucose, insulin and leptin, but not adiponectin. EPA/DHA increased plasma adiponectin levels, independent of food intake, reflecting the stimulation of Adipoq expression in adipocytes and the release of adiponectin from WAT, particularly from epididymal fat. Expression of Lep and the release of leptin from WAT, while being extremely sensitive to caloric restriction, was unaltered by EPA/DHA. Conclusions/interpretation: Intake of diets rich in EPA and DHA leads to elevated systemic concentrations of adiponectin, largely independent of food intake or adiposity and explain, to some extent, their anti-diabetic effects.